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27 Cards in this Set
- Front
- Back
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5 causes of tissue hypoxia
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ischemia, hypoxemia, ETC block, uncoupled ETC, AV shunts
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Ultimate effects of tissue hypoxia
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No O2 to accept electrons in ETC, no production of ATP. Na/K pump fails and cell swells (reversible change). Ribosomes fall from RER. Disruption of cell membrane and mitochondria induces apoptosis.
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Effects of low ATP in cell
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Increased glycolysis to support ATPase pump. Anaerobic glycolysis produces lactate with decreased intracellular pH which denatures proteins (coagulation necrosis), cell swelling, entry of calcium and apoptosis
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Pathophysiology of cell injury in hypoxia
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ETC fails due to lack of oxygen; 2. No ATP production in ETC increases anaerobic glycolysis (high citrate and AMP activate PFK-1); 3. increased lactate decreases cell pH which denatures proteins and produces coagulation necrosis; 4. ATPase fails and cell swells with fall off of ribosomes from RER; 5. disruption of cell membrane with entry of Ca activates phspholipase (lipid peroxidation), complement activation, nuclear enzymes with pyknosis and destruction of mitochondria and apoptosis
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What is methhemoglobin?
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Hemoglobin with oxidized (Fe3+) iron that cant bind O2. Decreases SaO2 and produces cyanosis. Caused by nitro/sulfa compounds. Rx.: methylene blue
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Increased PACO2, decreased PaO2, decreased O2 content, decreased SaO2
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Respiratory acidosis
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Normal PaO2 and SaO2, decreased Hb
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Anemia
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Normal Hb, PaO2, decreased SaO2, decreased O2 content
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CO poisoning or methhemoglobinemia
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CO poisoning tissue hypoxia
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Decreased O2 content and SaO2, normal PaO2, left shift of dissociation curve and cytochrome oxidase inhibition all cause hypoxia. Produced by car exhaust, heaters, smoke inhalation, wood stoves. Rx.: 100% O2. First symptom: headache
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Factors that left-shift O2 dissociation curve and decrease P50
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Decreased 2,3BPG, CO, MetHb, HbF, hypothermia, alkalosis
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Factors that right-shift O2 dissociation curve and increase P50
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Increased 2,3BPG, fever, acidosis
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Causes of hypoxia with normal O2 content
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Ischemia, cyanide poisoning, ETC uncouplers (alcohol, salicylates, dinitrophenol)
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Free radical metabolism
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NADPH oxidase and spontaneous superoxide, Superoxide dismutase makes H2O2 from superoxide. Catalase breaks down H2O2. Gluthathione reductase and GSH peroxide breakdwon H2)2 using reduced GSH and NADPH from G6PDH in HMP shunt
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Causes of free radical injury
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Aging process produces lipofuscin which peroxidates membrane; MPO system, O2 free radicals, ionizing radiation, acetaminophen (treat with acetylcyteine), CCl4 poisoning
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Features of apoptosis
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Eosinophilic cytoplasm; pyknotic nucleus, no inflamatory infiltrate
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Physiologic examples of apoptosis
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Thymus involution, Mullerian and Wolffian structure involution, gravid uterus
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Pathologic examples of apoptosis
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Councilman bodies in viral hepatitis, psammoma bodies, cancer
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Coagulation necrosis
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Denaturing and coagulation of proteins in cytoplasm (infarction). Pale Vs. hemorrhagic infarcts
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Liquefactive necrosis
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Neutrophil destruction with hemolytic enzymes. Abesesses, wet gangrene, brain, pancreas
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Caseous necrosis
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Combination of coagulation and liquefaction necrosis. Cheese-like material, casseating granulomas with macrophages
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Fat necrosis
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Lipases on fatty tissue. Pancreas. Chalky-white appearance
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Fibrinoid necrosis
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Histologically resembles fibrin. Eosinophilic mitral valve vegetations, immunocomplexes
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Fatty liver change
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In alcoholics - liver stores excess tryglycerides because increased NADH produces glycerol 3P and increased acetate (acetyl CoA) increases FA synthesis. In kwashiorkor, no apolipoproteins for VLDL
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Regulation of apoptosis
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Genes bcl-2 (inhibits apoptosis) prevents release of cytochrome C and binds protease activating factor (Apaf-1); p53 stimulates apoptosis. Mediated by caspases. Stimulated by cell injury, lack of hormones, Fas and TNF
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Rb suppressor gene and Rb protein
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Located on chromosome 13. Produces unphosphorylated Rb protein which stops cell from entering S phase. Phosphorylation by cyclin D/cdk complex allows it to enter S phase. Mutation of Rb gene produces cancer
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cdk/cyclin D complex
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When activated it phosphorylates Rb protein allowing cell to enter S phase
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p53 suppressor gene
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Located on chromosome 17. Produces a protein that inactivates cyclin D/cdk complex preventing Rb protein phosphorylation which keeps cell in G1
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